HSV-1 inhibits melanogenesis of PIG1 cells through downregulation of VN1R5/ERK pathway

IF 1.8 4区医学 Q3 DERMATOLOGY

Archives of Dermatological Research Pub Date : 2025-02-06 DOI:10.1007/s00403-025-03844-5

Yuxin Feng, Shibin Jiang, Jinping Yuan, Kun Zhou, Yansong Lu, Fenglin Zhuo, Xing-Hua Gao, Hong-Duo Chen, Rui-Qun Qi, Yan Wu

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Abstract

Herpes simplex virus type 1 (HSV-1) is an ubiquitous pathogen that can infect humans through skin or mucous regions. This study was to explore the effects and underlying mechanism of HSV-1 as examined within the human epidermal melanocyte cell line, PIG1. Our results showed that following HSV-1 infection, PIG1 cells shrank and acquired a rounded shape, while the numbers and lengths of their dendrites decreased and melanogenesis was inhibited. Meanwhile, the HSV-1 receptors (nectin-1, herpes virus entry mediator, paired immunoglobulin-like type 2 receptor alpha) and phospho-extracellular signal-regulating kinase (p-ERK) were all substantially decreased, while vomeronasal type-1 receptor 5 (VN1R5) increased. Results of RNA interference and protein inhibitor assays revealed that knockdown of VN1R5 increased the expression of p-ERK and microphthalmia-associated transcription factor (MITF), while an inhibition of ERK decreased VN1R5 expression. Taken together, our study provides the first evidence that HSV-1 can infect human normal melanocytes and inhibit melanogenesis through VN1R5/ERK pathway.

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来源期刊

Archives of Dermatological Research 医学-皮肤病学

CiteScore

4.10

自引率

3.30%

发文量

审稿时长

4-8 weeks

期刊介绍： Archives of Dermatological Research is a highly rated international journal that publishes original contributions in the field of experimental dermatology, including papers on biochemistry, morphology and immunology of the skin. The journal is among the few not related to dermatological associations or belonging to respective societies which guarantees complete independence. This English-language journal also offers a platform for review articles in areas of interest for dermatologists and for publication of innovative clinical trials.